Journal
JOURNAL OF NEUROTRAUMA
Volume 18, Issue 11, Pages 1195-1206Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/089771501317095232
Keywords
brainstem; coma; controlled cortical impact; dog; fluid percussion; head injury; ICP; impact acceleration; pig; primate
Funding
- NICHD NIH HHS [T32-HD40686] Funding Source: Medline
- NINDS NIH HHS [NS38087] Funding Source: Medline
- PHS HHS [30318] Funding Source: Medline
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Despite considerable investigation in rodent models of traumatic brain injury (TBI), no novel therapy has been successfully translated from bench to bedside. Although well-described limitations of clinical trails may account for these failures, several modeling factors may also contribute to the lack of therapeutic translation from the laboratory to the clinic. Specifically, models of TBI may omit one or more critical, clinically relevant pathophysiologic features. In this invited review article, the impact of the limited incorporation of several important clinical pathophysiologic factors in TBI, namely secondary insults (i.e., hypotension and/or hypoxemia), coma, and aspects of standard neurointensive care monitoring and management strategies (i.e., intracranial pressure [ICP] monitoring and ICP-directed therapies, sedation, mechanical ventilation, and cardiovascular support) are discussed. Comparative studies in rodent and large animal models of TBI (which may, in some cases, represent super models) are also presented. We conclude that therapeutic breakthroughs will likely require a multidisciplinary approach, involving investigation in a range of models, including clinically relevant modifications of established animal models, along with development and application of new innovations in clinical trial design.
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